{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T08:26:49Z","timestamp":1790670409265,"version":"4.1.0"},"reference-count":68,"publisher":"MDPI AG","issue":"21","license":[{"start":{"date-parts":[[2021,11,1]],"date-time":"2021-11-01T00:00:00Z","timestamp":1635724800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"United States (U.S.) Department of Veterans Affairs Biomedical Laboratory R&amp;D (BLRD) Service","award":["I01 BX004372"],"award-info":[{"award-number":["I01 BX004372"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>The concept of bladder ischemia as a contributing factor to detrusor overactivity and lower urinary tract symptoms (LUTS) is evolving. Bladder ischemia as a consequence of pelvic arterial atherosclerosis was first documented in experimental models and later in elderly patients with LUTS. It was shown that early-stage moderate ischemia produces detrusor overactivity, while prolonged severe ischemia provokes changes consistent with detrusor underactivity. Recent studies imply a central role of cellular energy sensors, cellular stress sensors, and stress response molecules in bladder responses to ischemia. The cellular energy sensor adenosine monophosphate-activated protein kinase was shown to play a role in detrusor overactivity and neurodegeneration in bladder ischemia. The cellular stress sensors apoptosis signal-regulating kinase 1 and caspase-3 along with heat shock proteins were characterized as important contributing factors to smooth muscle structural modifications and apoptotic responses in bladder ischemia. Downstream pathways seem to involve hypoxia-inducible factor, transforming growth factor beta, vascular endothelial growth factor, and nerve growth factor. Molecular responses to bladder ischemia were associated with differential protein expression, the accumulation of non-coded amino acids, and post-translational modifications of contractile proteins and stress response molecules. Further insight into cellular stress responses in bladder ischemia may provide novel diagnostic and therapeutic targets against LUTS.<\/jats:p>","DOI":"10.3390\/ijms222111862","type":"journal-article","created":{"date-parts":[[2021,11,1]],"date-time":"2021-11-01T22:21:34Z","timestamp":1635805294000},"page":"11862","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":19,"title":["Cellular Stress and Molecular Responses in Bladder Ischemia"],"prefix":"10.3390","volume":"22","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8732-0175","authenticated-orcid":false,"given":"Jing-Hua","family":"Yang","sequence":"first","affiliation":[{"name":"Department of Surgery, Boston University School of Medicine, Boston, MA 02118, USA"},{"name":"Proteomics Laboratory, VA Boston Healthcare System, Boston, MA 02130, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0103-3889","authenticated-orcid":false,"given":"Han-Pil","family":"Choi","sequence":"additional","affiliation":[{"name":"Proteomics Laboratory, VA Boston Healthcare System, Boston, MA 02130, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wanting","family":"Niu","sequence":"additional","affiliation":[{"name":"Research Section, VA Boston Healthcare System, Boston, MA 02130, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kazem M.","family":"Azadzoi","sequence":"additional","affiliation":[{"name":"Departments of Urology and Pathology, VA Boston Healthcare System and Boston University School of Medicine, Boston, MA 02130, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2021,11,1]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"535","DOI":"10.1161\/CIRCRESAHA.115.307611","article-title":"Epidemiology of Atherosclerosis and the Potential to Reduce the Global Burden of Atherothrombotic Disease","volume":"118","author":"Herrington","year":"2016","journal-title":"Circ. 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